骨髓间充质干细胞对急性肝衰竭大鼠肠源性内毒素血症的保护作用

目的探讨骨髓间充质干细胞(BMSCs)对硫代乙酰胺(TAA)所致急性肝衰竭大鼠肠源性内毒素血症(IETM)的保护作用。方法取雄性Wistar大鼠的骨髓贴壁培养获得BMSCs,取30只雌性Wistar大鼠随机分为正常组、TAA模型组和BMSCs治疗组,每组10只。TAA300mg/kg灌胃建立急性肝衰竭模型,24h后重复灌胃,正常组给予磷酸盐缓冲液(PBS)2ml灌胃,第2次灌胃后将BMSCs经尾静脉注射到BMSCs治疗组中,正常组和TAA模型组给予等量PBS注射。BMSCs治疗72h后处死。腹主动脉采血,检测血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)以及血浆内毒素含量,取部分肝组织及回肠作常规病理切片检查。结果与正常组比较,TAA模型组大鼠血清ALT,AST活性以及血浆内毒素水平均显著上升(P<0.05),BMSCs治疗组大鼠血清ALT,AST活性以及血浆内毒素水平与模型组相比均显著降低(P<0.05)。肝脏病理切片显示BMSCs能够明显减轻TAA对肝组织的炎症性破坏。结论 BMSCs尾静脉移植对TAA引起的急性肝衰竭大鼠IETM有一定的保护作用。

Transplantation of bone marrow mesenchymal stem cells protect against intestinal endotoxemia induced by acute liver failure in rats

Objective To explore the protective effect of bone marrow mesenchymal stem cells （BMSCs） trans- plantation against intestinal endotoxemia （IETM） from thioacetamide-induced （TAA） acute liver failure in rats. Meth- ods The BMSCs were purified and amplified by adherent culturing in vitro from bone marrow of male Wistar rats. Thirty female Wistar rats were randomly assigned to control group, thioacetamide model group and BMSC treated group （n=10）. The rat models of acute liver failure were induced by gavage of 300 mg/kg TAA in two consecutive days, while the normal group received gavage of 2 ml PBS at the same time. After the second gavage, the BMSC treated group was given caudal injection of BMSCs while the normal and TAA groups were injected with same volume of PBS. All rats were sacrificed at 72 hours after BMSCs transplantation. The serum ALT and AST, and plasma endotoxin （ET） levels were measured. The liver and ileum tissues were collected and examined for routine pathohistology. Results The lev- els of ALT, AST and ET were significantly increased in the TAA model group compared with the normal group （P 0.05）, and in the BMSCs group compared with the TAA model group （P0.05）. Pathological study showed notably less inflammatory damage in rat liver tissues associated with BMSC transplantation. Conclusion Caudal transplantation of BMSC appeared protective against IETM in rats with TAA-induced acute liver failure.